Evidence map›Paper›PMID 24667623›Full record

ArticleShock (Augusta, Ga.)2014

Gamma delta T cells regulate wound myeloid cell activity after burn.

Meenakshi Rani, Qiong Zhang, Martin G Schwacha

Open access · greenAbstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Skin Resident T Cell Interactions with NPY1RbioRxiv : the preprint server for biology · 2025
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Immunological approaches and therapy in burns (Review).Experimental and therapeutic medicine · 2020
    Review
  12. The role of the immune system during regeneration of the central nervous system.Journal of immunology and regenerative medicine · 2020
    Article
  13. Review
  14. Article
  15. The systemic immune response to pediatric thermal injury.International journal of burns and trauma · 2018
    Review
  16. Review
  17. The Healing Effect of N-Hexan- Dichloromethane Extract RootWorld journal of plastic surgery · 2018
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Meenakshi Rani*Department of Surgery, The University of Texas Health Science Center, San Antonio; and †US Army Institute of Surgical Research, Fort Sam Houston, Texas.
Qiong Zhang
Martin G Schwacha
The University of Texas Health Science Center at San Antonio · US

Funding

IMMUNOPATHOLOGICAL ASPECTS OF THREMAL INJURYR01GM079122 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SCHWACHA, MARTIN G · 2007 to 2011
$1.0M
NIGMS NIH HHS GM079122NIGMS NIH HHS R01 GM079122
6 · The paper itself

Abstract

Major burns induce immune complications, which are associated with myeloid cell activation by ill-defined mechanisms. Although γδ T cells have been shown to be important in postinjury inflammation and wound healing, their role in the regulation of myeloid cells remains unknown. To study this, wild-type (WT) and γδ T cell-deficient (δTCR) mice were subjected to major burn (25% total body surface area, third degree) or sham treatment. At 3 days thereafter, skin samples were assayed for cytokine content or used to isolate single cells that were used for myeloid cell characterization by flow cytometry. The number of CD11b myeloid cells increased by approximately 75% in the wound skin of WT mice. This influx was caused by increased myeloid-derived suppressor cells (CD11b GR1) whose numbers increased 19-fold compared with those of sham skin. In contrast, macrophage (MØ; CD11b F4/80) numbers decreased by approximately 50% after burn. In δTCR mice, burn increased the myeloid cell numbers approximately 5-fold. The increase in myeloid cells at the injury site of δTCR mice was caused by both a myeloid-derived suppressor cell (50-fold) and a MØ (2-fold) influx. Burn increased skin cytokine levels for a number of prototypic inflammatory cytokines (interleukin 1β, interleukin 6, tumor necrosis factor-α, macrophage inflammatory protein [MIP] 1β, etc). Tumor necrosis factor-α, MIP-1α, and MIP-1β levels were further elevated (2- to 3-fold) in the injured skin of δTCR mice compared with those of WT mice. In conclusion, these data show that γδ T cells regulate myeloid cell infiltration of the wound site and act to quell inflammation, thereby promoting the transition to the proliferative phase of wound healing.

Indexed as

AnimalsBurnsCD11b AntigenCell CountCell MovementCytokinesImmune ToleranceInflammation MediatorsMacrophagesMaleMice, Inbred C57BLMyeloid CellsReceptors, Antigen, T-Cell, gamma-deltaSkinT-Lymphocyte SubsetsWound HealingCD11b AntigenCytokinesInflammation MediatorsReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID24667623
PMCPMC4101017
OpenAlexW1980503050

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.